Alzheimer’s Society Condemns Daylight Robbery And Drugging Of Older People

Older people in Britain are being drugged and robbed when they need care.

Alzheimer’s Society accused the government of ‘daylight robbery’ and warned of a ‘Granny Crunch’ unless swift action is taken to change the system. Speaking today at the Annual Meeting of the Royal College of Psychiatrists, Chief Executive, Neil Hunt will call on the government to publish its review of the use of antipsychotic drugs and its green paper on adult funding of social care.

Neil Hunt, Chief Executive of Alzheimer’s Society, says

‘It’s an outrage that promises remain unfulfilled while people are being prescribed harmful antipsychotic drugs and families are being bankrupted by a derelict charging system. We are headed for a Granny Crunch unless the government acts now.

‘The average employed person works 1701 hours a year towards a healthy happy retirement. But for hundreds of thousands of older people who develop dementia the reality is starkly different. People become victims of daylight robbery as they are forced to pay huge amounts for often poor quality care. Care homes cost five times the state pension and quality varies greatly.

Over 105,000 people are inappropriately prescribed antipsychotic drugs, costing over ??60 million a year. These drugs double the risk of death, triple risk of stroke and accelerate cognitive decline.’

Alzheimer’s Society is calling for swift action to implement fairer charging systems and a plan to reduce the use of antipsychotics. In just 17 years over a million people in the UK will have dementia.


- The typical person with dementia in a care home has just 2 minutes social interaction with any another person every 6 hours[1].

- Over 70% of people with dementia experience challenging behavior at some point during their illness, such as aggression or restlessness. Specialist dementia training for care home staff reduces need for antipsychotics by up to 50%, according to Alzheimer’s Society research.

- People with dementia and carers are hit hardest by the charging system as; most dementia care is means tested as it comes from local authorities not the NHS; people need help for a long periods of time; most end of life dementia care is especially intensive and provided in care homes which is means tested.

- The basic state pension (per week from 9 April 2009)) based on your own or your late husband’s, wife’s or civil partner’s NI contributions is ??95.25.

- Saga Annual Cost of Care Report 2008 commissioned from Laing & Buisson found that the average cost of a care home per week was ??540. Figures are based on fees reported by 1,644 of the 11,878 registered private and voluntary care homes for older people in the UK responding to Laing & Buisson surveys between April and June 2008, plus minimum and maximum fee rates contained in inspection reports published by the Commission for Social Care Inspection in England.

- OECD (1998) data found that the average UK person works 1701 hours per year.

- One in three of us over 65 will die with dementia.

- 700,000 people in the UK have a form of dementia, more than half have Alzheimer’s disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.

- Alzheimer’s Society champions the rights of people living with dementia and those who care for them. Alzheimer’s Society works in England, Wales and Northern Ireland.

- Alzheimer’s Society needs to raise money to support people today and to find a cure for tomorrow. You can donate now by calling 0845 306 0898 or visiting alzheimers.

Alzheimer’s Society

Patients With Brain Injury May Benefit From Neuroscience Research

New neuroscience research by life scientists from UCLA and Australia may potentially help people who have lost their ability to remember due to brain injury or disease.

By examining how we learn and store memories, these scientists have shown that the way the brain first captures and encodes a situation or event is quite different from how it processes subsequent similar events.

The study is published in a recent edition of the online journal PLoS ONE, a publication of the Public Library of Science

Memories are formed in the part of the brain known as the hippocampus, a seahorse-shaped structure that plays critical roles in processing, storing and recalling information. The hippocampus is very susceptible to damage through stroke or lack of oxygen and is critically involved in Alzheimer’s disease, said study co-author Michael Fanselow, a UCLA professor of psychology and a member of the UCLA Brain Research Institute.

When a memory is first formed, a small protein involved in synaptic transmission – the NMDA receptor – is indispensable to the process, said study co-author Bryce Vissel, a group leader of the neuroscience research program at Sydney’s Garvan Institute of Medical Research. Activation of the NMDA receptor allows calcium to enter a neuron, and calcium permeability enables a chain of molecular reactions that help encode experience and consolidate memory, Fanselow and Vissel said.

Learning theorists have assumed that learning cannot occur without NMDA receptors. But the new findings show that NMDA receptors are not essential in “second-learning,” when the rules of “first-learning” are applied to new yet similar scenarios. Instead, another class of receptors known as AMPA receptors, also calcium permeable, appears to take up the task.

Although the findings are still preliminary, Fanselow is optimistic about what it could mean for people whose memory formation has been impaired.

“The system we are working with is one that we know is critically involved in Alzheimer’s disease and other kinds of brain deficit memory impairment,” he said. “This is just the start. We have uncovered a mechanism that contributes to learning and memory, and we now have to figure out what to do with it. When is it important normally? When can we harness it to take over function when the normal mechanisms aren’t working? Can we use it to have some protective effect in conditions like Alzheimer’s disease, where neurons are dying? Can we stimulate these pathways and keep them participating in memories?

“We can see that we might now have a target for drugs that are different from the standard class of cognitive enhancers,” he added. “We can see the possibilities for different styles of training that better activate this newly discovered mechanism.”

If the processes involved in second-stage learning can be mimicked therapeutically, he said, the health benefits potentially could be substantial.

Fanselow and Vissel have worked closely over the last six years, along with Thomas O’Dell, a UCLA professor of physiology at the David Geffen School of Medicine at UCLA, to unravel the two different synaptic mechanisms and their meanings.

“When we started this research, we knew that the NMDA receptor was implicated in learning and memory, and we decided to see if we could mimic its process through another receptor system,” said Vissel, a molecular neuroscientist. “Instead of having to create a new receptor system, we discovered one already in existence – one that was NMDA-independent. This amounted to uncovering a whole new mechanism of learning.”

Co-authors on the research are Stephen Heinemann (Salk Institute); Susumu Tonegawa (Massachusetts Institute of Technology); Brian Wiltgen (University of Virginia); Gordon Royle, Andrea Abdipranoto, and Nopporn Thangthaeng (Garvan Institute); and Erin Gray, Nate Jacobs and Faysal Saab (UCLA).

The research was federally funded by the National Institute of Mental Health and the National Science Foundation.

Stuart Wolpert
University of California — Los Angeles

Grant To Yale From Simons Foundation To Explore Genetic Causes Of Autism

Researchers at the Yale School of Medicine Child Study Center and 10 other institutions will share a $10 million gift from James and Marilyn Simons of The Simons Foundation to create a databank of DNA samples from autism patients around the country.

The goal is to collect a total of 3,000 samples from autism patients around the country to help identify different variants of autism and develop treatments. The principal investigators at Yale, Ami Klin and Matthew State, M.D., have received $1.2 million for three years to collect DNA samples from patients completing clinical evaluations or research protocols at the Autism Program at the Yale Child Study Center.

Autism is a complex brain disorder that inhibits a person’s ability to communicate and develop social relationships, and it is often accompanied by extreme behavioral challenges. Autism Spectrum Disorders are diagnosed in one in 150 children in the United States and affects four times as many boys as girls. Researchers do not know how many subtypes of autism exist. Klin, the Harris Associate Professor of Child Psychology and Psychiatry at Yale, said the gene data might help identify meaningful subtypes of autism, thus advancing knowledge that is critical for behavioral and brain studies, and promoting treatments that will likely be more specific to an individual’s variant of autism.

Other universities participating in the DNA databank collection include Harvard, Columbia, Emory, McGill, Boston, Washington University, the University of Washington, the University of Illinois-Chicago and the University of California, Los Angeles.

The Simons Consortium represents the most comprehensive and detailed effort to date to relate genotypic and phenotypic data in autism. Subjects completing the protocol will have the most refined genotypic analyses that can then be related to a wealth of data on the affected individuals themselves and on their family members. The Consortium will house the data in a centralized repository that will be accessible to researchers within and outside the institutions involved in this effort.

The Simons Foundation is a private family foundation based in New York City. The primary mission is to fund advanced research in science and mathematics. A secondary mission is to help children with learning differences. Bridging these two areas, the Simons Foundation has recently undertaken a major initiative supporting research into autism and its treatment. The Foundation aims to spend $100 million long-term to find a cure for the developmental disorder.


39th Annual Society For Neuroscience Conference

Neuroscience researchers from the Yerkes National Primate Research Center, Emory University, are presenting a wide range of research topics at the Society for Neuroscience’s 39th annual meeting in Chicago, Oct. 17-21, 2009. The information below is a representation of the neuroscience research Yerkes scientists will be discussing. To learn more about ongoing research and scientific resources available at the Yerkes Research Center and the other seven national primate research centers, please visit exhibit booth 2153.

Stuart Zola, PhD, Director, Yerkes National Primate Research Center, and one of the nation’s leading neuroscientists, moderated the Dialogues between Neuroscience and Society series Saturday, Oct. 17, 11 a.m. – 1 p.m. This series offers thought-provoking perspective on issues of interest and/or concern to neuroscientists by engaging with leaders from other fields of study.

Todd Preuss, PhD, researches the evolutionary specializations of the human brain by comparing humans to chimpanzees and to other nonhuman primates. The goal is to understand the extent to which evolutionary expansion of the human brain was accompanied by the addition of new areas or by the enlargement and internal reorganization of existing areas. Preuss participated in a news conference entitled “Evolution of Brain and Behavior” Sunday, Oct. 18 at 12:30 p.m. Preuss will also present a poster presentation Tuesday, Oct. 20, 3 p.m. – 4 p.m.

The Yerkes Research Center is sponsoring the Meet the Expert session on imaging that will feature John Gabrielli of MIT, one of Yerkes’ Scientific Advisory Board members. This session was Saturday, October 17, 9:30 a.m. – 10:45 a.m.

Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease and Other Neurodegenerative Diseases

Lary Walker, PhD, studies Alzheimer’s disease, stroke and trauma, the aging process and prion diseases. Walker’s current research focuses on the protein structure and chemistry of Alzheimer’s disease as well as the disease pathogenesis. He is also studying amyloid deposits in Alzheimer’s affected brains and evaluating the efficacy and side effects of therapeutic immunizations. Walker lab poster presentation: Rebecca Rosen, PhD, Sunday, Oct. 18, 2 p.m. – 3 p.m.

Stella Papa, PhD, researches the areas of pathophysiology and therapeutics of neurodegenerative disorders focusing on Parkinson’s disease and other movement disorders. Papa lab poster presentation: S. Uthayathas, Tuesday, Oct. 20, 9 a.m. – 10 a.m.

Yoland Smith, PhD, researches the neurochemical changes that mediate cell death and abnormal motor behaviors in neurodegenerative diseases, such as Parkinson’s disease and Huntington’s chorea. Smith will present a poster Tuesday, Oct. 20, 11 a.m. – noon.

Thomas Wichmann, MD, who collaborates with Smith, researches the pathophysiology of movement disorders, such as Parkinson’s disease. His research focuses on evaluating the role of abnormal nerve cell activity in the basal ganglia in the development of Parkinsonian motor signs. The goal of his work is to gain a better understanding of the chemical and electrophysiologic changes that cause Parkinson’s that can then be translated into new and more effective therapies. Smith and Wichmann lab poster presentations are scheduled for Wednesday, Oct. 21: J.G. Masilamoni, 1 p.m. – 2 p.m.; Abraham Mathai, 2 p.m. – 3 p.m.; Jean-Francois Pare, 3 p.m. – 4 p.m.; Kalynda Gonzales, 4 p.m. – 5 p.m.; and Rosa Villalba PhD, 4 p.m. – 5 p.m.


Yerkes Director Dr. Zola researches the brain structures important for memory and seeks to determine how these structures separately and in combination contribute to memory function. His lab also studies emotional behavior and its link to memory function in humans and animals. Zola will present a poster Tuesday, Oct. 20, 2 p.m. – 3 p.m.

Jocelyne Bachevalier, PhD, studies infantile amnesia, the inability to remember virtually anything from infancy. The primary goal of her research program is to determine the structural or functional immaturity responsible for infantile amnesia. Her lab also studies the nature of the memory decline in monkeys, which accompanies normal aging, to help explain aging-related memory disorders. Bachevalier lab poster presentations: Jessica Raper, Saturday, Oct. 17, 1 p.m. – 2 p.m.; Alyson Zeamer, Saturday, Oct. 17, 2 p.m. – 3 p.m.; Shala Blue, Saturday, Oct. 17, 3 p.m. – 4 p.m.; and Laetitia Cirilli, Tuesday, Oct. 20, 11 a.m. – noon.

Elizabeth A. Buffalo, PhD, researches the neuronal mechanisms involved in the establishment and maintenance of memory. Through her research, she records neural activity in monkeys that have been trained to perform various types of memory tasks and investigates how changes in neuronal activity correlate with each monkey’s ability to learn and remember in order to better understand how medial temporal lobe circuits support memory formation. Such understanding has the potential to make way for new therapies aimed at reducing or preventing memory loss that results from medial temporal lobe disease. Buffalo lab poster presentation: Megan Tompkins, Saturday, Oct. 18, 2 p.m. – 3 p.m.


Michael J. Kuhar, PhD, chair of Yerkes’ Division of Neuroscience, studies drug addiction and the role of CART peptides in the abuse of cocaine and other psycho-stimulate drugs. Kuhar’s ongoing research includes examining the biochemical and physiological mechanisms involved in drug abuse in order to develop potential medications and treatments for drug abusers. Kuhar lab poster presentations: G. Desbordes, Saturday, Oct. 17, 3 p.m. – 4pm.; George Rogge, Sunday, Oct. 18, 3 p.m. – 4pm.; Doug Jones, PhD, Sunday, Oct. 18, 4 p.m. – 5pm.; Yiming Lin, PhD, Monday, Oct. 19, 3 p.m. – 4 p.m.; and George Hubert, PhD, Wednesday, Oct. 21, 8 a.m. – 9 a.m.

Fear, Anxiety and Stress

Michael Davis, PhD, researches the physiological bases of learning and memory and brain areas involved in fear, anxiety and stress. Davis lab poster presentations are scheduled for Wednesday, Oct. 21: Leigh Miles, 1 p.m. – 2 p.m.; Ryan Parsons, 3 p.m. – 4 p.m.; D.L. Walker, 4 p.m. – 5 p.m.; and Kelly Sink, 4 p.m. – 5 p.m.

E. Christopher Muly, MD, PhD, researches how various forms of experience alter the structural organization of nerve cell communication to understand how experience and drugs mediate alterations in brain functioning relevant to a wide variety of neuropsychiatric disorders, including post traumatic stress disorder, Parkinson’s disease and schizophrenia. Muly lab poster presentation: S.V. Kusnoor, Tuesday, Oct. 20, 11 a.m. – noon.

Kerry Ressler, MD, PhD, studies the biological mechanisms that cause fear. Ressler focuses on post traumatic stress disorder, a condition that causes chronic anxiety and traumatic flashbacks, and the genetic and neurobiological keys to preventing and treating the disease. Ressler lab poster presentations were scheduled for Sunday, Oct. 18: Aaron Jasnow, 9 a.m. – 10 a.m.; Georgette Gafford, 11 a.m. – noon; Kimberly Maguschak, 3 p.m. – 4 p.m.; and Scott Heldt, 4 p.m. – 5 p.m.

Mar Sanchez, PhD, studies neurobiological systems that control stress physiology and emotion regulation in nonhuman primates, particularly the developmental effects of early adverse experiences on stress neuroendocrine systems, emotion regulation and related neurobiological substrates of primates. Sanchez will present a poster Monday, Oct. 19, 1 p.m. – 2 p.m. Sanchez lab poster presentation: Brittany Powell, Sunday, Oct. 18, 9 a.m. – 10 a.m.

Sex and the Brain

Larry Young, PhD, researches the molecular-, cellular- and systems-level mechanisms underlying social behaviors, specifically monogamy and partner bonding. Young’s research focuses on the roles of oxytocin and vasopressin in a variety of social behaviors in order to better understand the relationship between genes, the brain and behavior. Young lab poster presentations: Sara Freeman, Monday, Oct. 19, 1 p.m. – 2 p.m.; and Todd Ahern, Monday, Oct. 19, 4 p.m. – 5 p.m.


Graduate student Eric Hecht presented a poster on imaging Sunday, Oct. 18, 9 a.m. – 10 a.m. Hecht works in the labs of Dr. Preuss and Jim Rilling, PhD.

Emily Rios

Emory University

Repurposing Of Enbrel For Alzheimer’s Disease

At Cambridge Healthtech Institute’s Third Annual Drug Repositioning Summit on Monday, October 6 in Boston, the audience is scheduled to hear, as a Keynote Presentation, the story of how an individual physician has charted an entirely new course for a therapeutic which is already one of the most successful of all time.

Enbrel® (etanercept) has proven effective for treating a host of medical conditions, from rheumatoid arthritis to psoriasis, generating more than $4 billion dollars per year in revenue for its owner, Amgen. Yet despite this success Amgen has failed to initiate study of etanercept’s emerging off-label uses in the field of neurology, which could potentially address enormous unmet medical needs and help people throughout the world. Etanercept is one of a new class of medications, produced through biotechnology, which specifically neutralize an immune signaling molecule called TNF. Excess TNF is centrally involved in scores of diseases, including rheumatoid arthritis, Alzheimer’s, sciatica pain, and psoriasis. In Alzheimer’s disease excess TNF has been documented in the cerebrospinal fluid, and the rationale for anti-TNF treatment is supported by genetic, epidemiologic, basic science, and clinical data (1-11).

The Keynote Presentation, entitled “Repurposing of Enbrel for Alzheimer’s Disease” will be made by Edward Tobinick MD, Director of the Institute for Neurological Research, a private medical group, inc. in Los Angeles. Dr. Tobinick is the inventor and patent holder of the etanercept off-label indication for Alzheimer’s Disease, as well as more than 200 different inventions involving new off-label uses of TNF blockers, such as etanercept, in neurology, opthalmology, and for a variety of additional innovative clinical indications(12-17). Many of the novel uses of etanercept which Dr. Tobinick invented, beginning nearly a decade ago, such as for sciatica, Alzheimer’s, and myasthenia gravis, have subsequently been supported by peer-reviewed, published studies performed by independent researchers from academic centers across the globe(18-26).

As an example, a recently completed, double-blind, placebo-controlled study conducted by independent researchers at Johns Hopkins/Walter Reed Army Medical Center has confirmed the efficacy of etanercept for sciatica, using a patented, perispinal method of administration of etanercept which Dr. Tobinick invented(27).

Dr. Tobinick has been invited to and has presented his clinical and research findings at multiple prestigious medical research meetings, including this year’s International Congress on Alzheimer’s Disease (ICAD 2008), the 7th International Alzheimer’s Drug Discovery Conference; at the Karolinska Institutet in Stockholm, Sweden, the home of the Nobel Prize in medicine; and in multiple, peer-reviewed, published medical articles(1-5, 27-31).

His published, peer-reviewed scientific articles have been cited by more than 150 scientific publications from around the world(1-6, 18, 20, 23-25, 32, 33). In addition, his groundbreaking work has been recognized by the Dana Alliance for Brain Initiatives, the world’s leading organization of neuroscientists, which counts among its members ten Nobel Laureates(34); by leading journals, including Nature Clinical Practice Neurology(35); by the Faculty of 1000 Biology, the expert guide to the most important advances in biology(36); and featured in news articles from around the world(37-39). Despite the immense potential to help countless people, the great unmet medical need, and their enormous continuing revenue from etanercept sales, Amgen has yet to confirm its intention to begin even preliminary clinical study in this direction.

A failure to investigate is perhaps even more puzzling in view of the increasing scientific support from cutting edge research, which is in addition to the genetic studies which have identified excess TNF as a therapeutic target in Alzheimer’s(9, 10, 33, 40-43). For example, scientists from the Trinity College Institute of Neuroscience in Ireland have demonstrated that defects in hippocampal learning and memory mechanisms created by forms of amyloid are mediated by TNF(41-43). Perhaps even more significant is the recent identification of TNF as a gliotransmitter which regulates synaptic transmission in the brain(39, 44, 45).

The synaptic effects of TNF which regulate learning, memory, and neurotransmission provide a most exciting area for scientific research. These synaptic effects, which may occur with extreme rapidity, provide a rational and scientifically plausible explanation for the rapid clinical effects of etanercept which have been documented in multiple, peer-reviewed scientific studies and in multiple patients(1-5, 18, 28, 30). To ignore this new direction in scientific thinking, which recognizes the role of TNF not just in inflammation but also as an immune regulator of synaptic communication and other aspects of brain function, would be to impede scientific progress.

Fortunately, with the expiration of Amgen’s patents on etanercept approaching in 2012, other pharmaceutical companies will soon have the ability to explore these extraordinary discoveries which have the potential to help millions of patients around the world.

The Keynote Presentation will cover over ten years of research, highlighting the difficult hurdles which new breakthroughs in science and medicine must surmount before they are even considered by the scientific and medical communities.

For further information on this Keynote Presentation, please visit AlzheimerVideoNews , or the INR® website.

Institute for Neurological Research

View drug information on Enbrel.

Alzheimer’s Disease: Finding Has Implications For Host Of Neurodegenerative Diseases

Researchers from the University of Pennsylvania School of Medicine have shown, in unprecedented detail, how a small molecule is able to selectively take apart abnormally folded protein fibers connected to Alzheimer’s disease and prion diseases. The findings appeared online in the Proceedings of the National Academy of Sciences. Finding a way to dismantle misfolded proteins has implications for new treatments for a host of neurodegenerative diseases.

Abnormal accumulation of amyloid fibers and other misfolded forms in the brain cause neurodegenerative diseases. Similarly, build-up of abnormally folded prion proteins between neurons causes the human version of mad cow disease, Creutzfeldt-Jakob disease.

“Surprisingly, a small molecule called DAPH selectively targets the areas that hold fibers together, and converts fibers to a form that is unable to grow. Normally fibers grow from their ends, but the drug stops this activity,” says senior author James Shorter, PhD, Assistant Professor of Biochemistry and Biophysics. “Our data suggest that it is possible to generate effective small molecules that can attack amyloid fibers, which are associated with so many devastating diseases.”

The researchers are now working on how DAPH acts as a wedge to stop the fibers from growing. “Presumably DAPH fits very neatly into the crevices between fiber subunits,” explains Shorter. “When we grow yeast cells with the prion in the presence of DAPH, they begin to lose the prion. We also saw this in the test tube using pure fibers. The small molecule directly remodels fiber architecture. We’ve really been able to get at the mechanism by which DAPH, or any small molecule, works for the first time.” DAPH was originally found in a screen of small molecules that reduce amyloid-beta toxicity in the lab of co-author Vernon Ingram, Shorter’s collaborator at the Massachusetts Institute of Technology (MIT).

In a test tube, if a small amount of amyloid or prion fiber is added to the normal form of the protein, it converts it to the fiber form. But when DPAH is added to the mix, the yeast prion protein does not aggregate into fibers. “It’s essentially stopping fiber formation in its tracks,” says Huan Wang, first author and research specialist in Shorter’s lab. “We were surprised to see two very different proteins, amyloid-beta and Sup35, sensitive to this same small molecule.”

The next step is to identify more potent DAPH variants with greater selectivity for deleterious amyloids. Since some amyloids may turn out to be beneficial – for example, one form may be involved in long-term memory formation – it will be necessary to find a drug that does not hit all amyloids indiscriminately. “We’d need one that hits only problem amyloids, and DAPH gives us a hint that such selectivity is possible” says Shorter.

This work was initiated in Susan Lindquist’s lab at MIT and completed at Penn. The study was funded by the National Institute of General Medical Sciences, the Alzheimer’s Association, the Kurt and Johanna Immerwahr Fund for Alzheimer Research, a DuPont-MIT alliance, the American Heart Association, and pilot grants from the University of Pennsylvania Alzheimer’s Disease Core Center and Institute on Aging.

PENN Medicine is a $3.5 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System.

Penn’s School of Medicine is currently ranked #4 in the nation in U.S.News & World Report’s survey of top research-oriented medical schools; and, according to most recent data from the National Institutes of Health, received over $379 million in NIH research funds in the 2006 fiscal year. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

The University of Pennsylvania Health System includes three hospitals – its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation’s “Honor Roll” hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation’s first hospital; and Penn Presbyterian Medical Center – a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.

Source: Karen Kreeger

University of Pennsylvania School of Medicine

Risk Of Asthma Attacks Raised By Food Allergies

Food allergies are more common among people with asthma and may contribute to asthma attacks, according to one of the most comprehensive surveys of food allergies ever undertaken. National Jewish Health Associate Professor of Pediatrics Andrew H. Liu and his colleagues also report in the November 2010 Journal of Allergy and Clinical Immunology that food allergies are more prevalent among children, males and non-Hispanic blacks.

“Our study suggests that food allergies may be an important factor, and even an under-recognized trigger for severe asthma exacerbations,” said Dr. Liu. “People with a food allergy and asthma should closely monitor both conditions and be aware that they might be related.”

The researchers, funded by the National Institute of Environmental Health Sciences (NIEHS), analyzed data from 8,203 people, aged 1 to greater than 60, who completed the National Health and Nutrition Examination Survey in 2005-2006, and had their blood tested for antibodies to four specific foods: peanuts, milk, eggs and shrimp.

“This study is very comprehensive in its scope,” said Darryl Zeldin, MD, acting clinical director at the NIEHS and senior author on the paper. “It is the first study to use specific blood serum levels and look at food allergies across the whole life spectrum, from young children aged 1 to 5, to adults 60 and older.”

Depending on the IgE antibody levels found in participants blood, they were categorized as sensitized to one or more of the foods or not sensitized. The sensitized participants were subdivided into those with an unlikely (10-20 percent), possible (50 percent) and likely (greater than 95 percent) chance of having food allergies.

Likely food allergies were twice as common among participants who had ever received an asthma diagnosis as among those with no asthma diagnosis.

The odds of having food allergies grew with increasing severity of asthma. Those who currently have asthma were 3.8 times as likely to have food allergies as those who had previously been diagnosed with the disease but no longer had it. Those who had visited an emergency department for asthma in the past year were almost seven times as likely to have food allergies as those who had ever been diagnosed with asthma but not visited an emergency department. Overall, 15.8 percent of participants who had visited the emergency department for asthma had IgE levels indicating possible or likely food allergies.

Researchers could not determine if food allergies actually cause asthma attacks or if asthma and food allergies are both manifestations of a severe allergic profile. They speculated that food-allergic reactions might be triggered in some people with asthma only when combined with strenuous exercise.

Overall, the researchers estimate that 2.5 percent or 7.5 million Americans have food allergies. This estimate is lower than some estimates, but in line with many others. This study’s analysis of actual IgE antibody levels to foods in a large nationally representative sample lent authority to the results. However, since the tests measure potential allergies to only four of the most commonly allergenic foods, the results may slightly underestimate overall prevalence of food allergies, wrote the authors.

Children ages 1 to 19 were twice as likely to have food allergies as the general population. Non-Hispanic blacks were three times as likely to have food allergies, and males were twice as likely to have food allergies. Black male children were 4.4 times as likely to have food allergies.

Peanut allergy was the most common food allergy, affecting 1.3 percent of the surveyed population. Contrary to milk and egg allergies, which peaked in children under 5, peanut allergies were highest among children ages 6 to 19 (2.7 percent).

National Jewish Health is known worldwide for treatment of patients with respiratory, cardiac, immune and related disorders, and for groundbreaking medical research. Founded in 1899 as a nonprofit hospital, National Jewish remains the only facility in the world dedicated exclusively to these disorders. Since 1998, U.S. News & World Report has ranked National Jewish the #1 respiratory hospital in the nation.

William Allstetter
National Jewish Health

WFP Expands Aid To Victims Of Typhoon Reming In The Philippines

Continuing its assistance to victims of a typhoon which struck
the Philippines in late 2006, the United Nations World Food Programme
(WFP) has made available an additional 5,880 bags of rice (294 tons)
for distribution to families that lost their homes to Typhoon Reming.

The rice will be provided to nearly 6,000 families in Albay province,
many of whom are still living in evacuation camps more than two months
after the calamity, and will provide for their needs for at least a

“It takes time to rebuild after a disaster of this scale,” said Valerie
Guarnieri, WFP Country Director and Representative to the Philippines.
“The cameras have moved on to crises elsewhere, but WFP will stay with
the affected communities while they repair their fishing boats, plant
for the next harvest, or find new ways to make a living.”

Typhoon Reming (also called Durian) struck the Philippines on 30
November 2006, devastating the Bicol region. Most of the severely
affected areas are coastal and farming municipalities and towns located
around the periphery of Mt. Mayon Volcano in Albay province where more
than a thousand lives were lost and entire villages buried under mud and
boulders which careened down the slopes of the volcano.

Of the survivors, nearly one million people were displaced, many of whom
sought refuge in schools and other evacuation centers set up by the
Government, while others stayed near their homes or moved in with family
and friends.

While international aid has been forthcoming, more donor contributions
are still needed to support the relief and recovery of the victims of
Typhoon Reming. The UN Appeal for US$48.7 million to support food,
shelter, health, water, sanitation and recovery activities is only 11
percent funded, crippling the ability of the United Nations agencies and
their partners to respond.

WFP, along with Government and non-governmental organizations, recently
completed an emergency food security assessment. Preliminary findings
show that food assistance will be needed over the next several months,
particularly for people in evacuation centers and those whose
livelihoods are agriculture and fishery based.

The assessment also emphasized the need to regularize food distributions
to affected communities, and to offer increased rations. Previously,
most assisted families received only 2 kg of rice along with small
quantities of beans, canned sardines and noodles which, while welcome,
fell considerably short of their requirements. The typical Filipino
family consumes from 10 to 15 kg of rice each week.

With the newly agreed allocation from WFP, families will receive a 50 kg
sack of rice, which they can supplement with small amounts of
vegetables, beans or fish. WFP purchased the rice locally and it is
being distributed by local government and non-governmental

A WFP office established in Legaspi in January monitors food
distributions and coordinates food relief and recovery efforts with
Government and other partners. More than 30,000 family members will
benefit from this additional food assistance, according to WFP.

This latest assistance brings to 440 tons (8,800 bags) of food relief
provided by WFP to bolster typhoon relief efforts, funded by the UN
Central Emergency Response Fund. WFP has also requested a total of
US$3.1 million (5,788 tons of rice, beans and vegetable oil) from donors
as part of the United Nations Emergency Response Typhoon Appeal. So far,
Canada has donated CDN$1 million (US$850,000).

WFP had operations in the Philippines from 1965-1996 and resumed its
activities in 2006 to support the peace process and help meet the needs
of the most vulnerable people in Mindanao. In addition to the Mindanao
programme, which seeks to assist 2.1 million conflict-affected people,
WFP remains ready to assist with national disaster response efforts when

WFP is the world’s largest humanitarian agency: each year, we give food
to an average of 90 million poor people to meet their nutritional needs,
including 58 million hungry children, in at least 80 of the world’s
poorest countries.

WFP Global School Feeding Campaign – For just 19 US cents a day, you can
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Memory Test And PET Scans Detect Early Signs Of Alzheimer’s

A large study of patients with mild cognitive impairment revealed that results from cognitive tests and brain scans can work as an early warning system for the subsequent development of Alzheimer’s disease.

The research found that among 85 participants in the study with mild cognitive impairment, those with low scores on a memory recall test and low glucose metabolism in particular brain regions, as detected through positron emission tomography (PET), had a 15-fold greater risk of developing Alzheimer’s disease within two years, compared with the others in the study.

The results, reported by researchers at the University of California, Berkeley, on Tuesday, July 14, at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease in Vienna, Austria, are a major step forward in the march toward earlier diagnoses of the debilitating disease.

“Not all people with mild cognitive impairment go on to develop Alzheimer’s, so it would be extremely useful to be able to identify those who are at greater risk of converting using a clinical test or biological measurement,” said the study’s lead author, Susan Landau, a post-doctoral fellow at UC Berkeley’s Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory.

“The field, in general, is moving toward ways to select people during earlier stages of Alzheimer’s disease, including those who show no outward signs of cognitive impairment,” said Dr. William Jagust, a faculty member of UC Berkeley’s Helen Wills Neuroscience Institute and principal investigator of the study. “By the time a patient is diagnosed with Alzheimer’s disease, there is usually little one can do to stop or reverse the decline. Researchers are trying to determine whether treating patients before severe symptoms appear will be more effective, and that requires better diagnostic tools than what is currently available.”

In the latest study, researchers compared a variety of measurements that had previously shown promise as early detectors of Alzheimer’s. The measurements included scores on the Auditory Verbal Learning Test; the volume of the hippocampus, the part of the brain associated with the formation of new memory; the presence of the apolipoprotein E4 gene, which has been linked to increased risk of Alzheimer’s; certain proteins found in the cerebrospinal fluid; and glucose metabolism detected in PET brain scans. A low rate of glucose metabolism in a particular brain region is considered a sign of poor neural function, most likely due to the loss of synapses in that area.

“What’s really novel about our study is that we evaluated all of these biomarkers in the same subjects, so we could more easily compare the predictive value of any one measure over the others,” said Landau. “The Auditory-Verbal Learning Test, which measures memory recall ability, and the PET scans measuring glucose metabolism were the two markers that clearly stood out over the others.”

The researchers pointed out that other measurements – in particular, hippocampus volume and the cerebrospinal fluid markers – also showed promise in predicting disease progression. However, when considering all the measurements together, PET scans and memory recall ability were the most consistent predictors. The researchers expect to have more complete information about which measures serve as the best predictors in a year as they continue to gather data for this ongoing study.

An earlier study led by Jagust, a professor with joint appointments at UC Berkeley’s School of Public Health and the Lawrence Berkeley National Laboratory, found that PET scans and magnetic resonance imaging (MRI) could detect neurological changes in asymptomatic people who subsequently developed dementia or mental impairment, although it was too soon to say if those people would go on to develop Alzheimer’s.

The research is part of the nationwide Alzheimer’s Disease Neuroimaging Initiative, a 60-center study funded by the National Institute on Aging. The ultimate goal of the initiative is to find a biomarker for Alzheimer’s that would predict individuals who will later develop Alzheimer’s disease. Ideally, this marker would be identifiable very early, even in individuals who do not yet show signs of mental impairment.

Jagust heads the initiative’s research on PET imaging. The UC Berkeley study includes those patients who had measures for all biomarkers.

Sarah Yang
University of California – Berkeley

Special Turmeric Extract Benefits Osteoarthritis Patients

A new clinical trial supports the benefits to people with osteoarthritis who used a unique extract of turmeric. [1] Scientists in Italy have studied the pain-relief, increased flexibility, and other effects of a special, patented extract of the roots of turmeric, the flavorful spice that has been used for centuries as a traditional remedy. Turmeric formulations have shown a wide range of safety and significant scientific and clinical benefits in recent animal research and human clinical trials. [2, 3]

The characteristic yellow color of turmeric, which is found in many yellow mustards and yellow curry preparations, derives from compounds known collectively as curcuminoids, whose most abundant member is curcumin. Curcumin is difficult to absorb into the human bloodstream from the gastrointestinal tract when consumed orally. [4]

Researchers in Italy selected 50 patients with X-ray diagnosed osteoarthritis in either one or both knees to evaluate if the special turmeric formulation called Meriva® could provide more benefits to their standard medical therapy. In this trial, the patients were split into two groups: the first one received standard medical treatment as determined by patients’ physicians, while patients in the second group added the special curcumin extract to their standard medical treatment.

After 90 days, the following benefits were observed: Compared to the controls, patients in the Meriva group experienced a 58 percent decrease in their overall pain, stiffness and physical functionality as measured by the widely used medical scoring method developed by Western Ontario and McMaster Universities (WOMAC). In addition, the Social and Emotional Index (SEI) score resulted in a greater than 300 percent improvement in Meriva patients compared to patients not taking the curcumin extract. Blood tests indicated that in patients having elevated levels of C-reactive protein (CRP), a 16-fold decrease of this inflammation marker was observed in the Meriva group. Finally, the subjects using Meriva were able to reduce their reliance on standard painkillers (NSAIDs, non-steroidal anti-inflammatory drugs) by 63 percent compared to patients on conventional medical therapy alone.

Taken together, these data show that Meriva turmeric extract improves the clinical benefit of a standard NSAIDs-based treatment of osteoarthritis, making it possible for patients to decrease their medication load and increase its efficacy.

Consistent with data from other human studies on various types of turmeric extracts, Meriva demonstrated a high degree of safety without producing any serious adverse side effects.

“This is great news for people who suffer from osteoarthritis and the physicians who treat them,” said Mark Blumenthal, Founder and Executive Director of the nonprofit American Botanical Council, an independent herbal medicine research and education organization in Austin, Texas.

“Turmeric has long been known to have anti-inflammatory and pain-relieving properties and this trial, on this special turmeric extract, is another important step towards validating the curcumin in turmeric as an increasingly popular herbal dietary supplement. When one considers the overall safety of turmeric extract and curcumin, especially compared to some of the pharmaceutical drugs which have had to be removed from the market due to serious safety concerns, the growing clinical evidence for the use of turmeric extract is compelling,” he added.

The authors of this trial write that “curcumin is one of the most extensively investigated products of natural origin. Its broad spectrum of bioactivity and low oral toxicity have expanded its use to several clinical conditions. Many potential beneficial properties of the natural product [i.e. curcumin] have not produced effective clinical results because curcumin shows a poor water solubility and stability, a low and unpredictable oral absorption, and a quick metabolism.” [1] Researchers believe that these problems have hampered the clinical development of curcumin as a pharmaceutical product and as a dietary supplement. Meriva has exhibited high levels of oral bioavailability in a previous comparative animal pharmacokinetic* study. [5]

The Meriva curcumin extract used in this clinical trial is a special patented combination of curcumin with soybean-derived phosphatidylcholine (1:2 ratio). Produced and distributed by Indena SpA of Milan, Italy, the world’s largest manufacturer of standardized botanical extracts for the food, dietary supplement, pharmaceutical and cosmetic industries. Meriva has recently been introduced into the market as a dietary supplement ingredient marketed in the USA and Europe. In this clinical study, Meriva capsules prepared by Thorne Research Inc. (Dover, Idaho, USA) were used at a dosage of 1 gram Meriva curcumin complex per day (standardized to contain 18-22 percent curcuminoids, and corresponding to 200 mg curcumin per day).

About Turmeric

Turmeric is a traditional spice, food and medicine, native to Southeast Asia, and widely used in Ayurvedic system of traditional medicine in India. Turmeric is made from the roots and rhizomes (lateral roots) of the turmeric plant, a member of the same plant family as ginger. According to a recent review article, over 2,500 preclinical scientific investigations have supported the activity of curcumin from turmeric as a potential agent to treat directly or as an adjunct treatment for various chronic diseases such as inflammatory diseases, some forms of cancer and possibly also Alzheimer’s disease. Turmeric’s popularity has risen tremendously in the past few years as consumers learn more about its safety and wide spectrum of health benefits. [2, 3] Turmeric dietary supplements were ranked 5th in sales in natural food stores in 2009, up about 23 percent from the previous year, generating over $10 million in sales in that market channel alone, according to a report in the American Botanical Council’s journal HerbalGram, based on information from SPINS, a market research firm which monitors sales of dietary supplements in the natural food channel of trade.


(1) Belcaro G, Cesarone MR, Dugall M, Pellegrini L, Ledda A, Grossi MG, Togni S, Appendino G. Product-evaluation registry of Meriva®, curcumin-phosphatidylcholine complex, for the complementary management of osteoarthritis. PanMinerva Med. 2010;52 (Suppl. 1 to No. 1):55-62.

(2) Aggarwal BB, Sung B. Pharmacological basis for the role of curcumin in chronic diseases: an age-old spice with modern targets. Trends Pharmacol Sci..2009;30:85-94.

(3) Engels G. Turmeric (Curcuma longa). HerbalGram 86:1-3.

(4) Anand P, Kunnumakkara AB, Newman RA, Aggarwal BB. .Bioavailability of Curcumin: Problems and Promises. Mol. Pharmaceutics: 2007;4(6):807-818.

(5) Marczylo T, Verschoyle R, Cooke D, Morazzoni P, Steward W, Gescher A, Comparison of systemic availability of curcumin with that of curcumin formulated with phosphatidylcholine. Chemother. Pharmacol. 2007;60:171-177.

(6) Cavaliere C, Rea P, Lynch ME, Blumenthal M. Herbal supplement sales rise in all channels in 2009. HerbalGram. 2010;86:62-65.

Source: American Botanical Council